Abstract

A total number of 104 Acinetobacter baumannii isolates obtained from a teaching hospital were studied for the genetic basis of their resistance to aminoglycosides. The rate of aminoglycoside-resistant A. baumannii was 76.9% (80/104), and 66.25% (53/80) aminoglycoside-resistant isolates were high-level resistant to either aminoglycosides including amikacin, gentamicin and tobramycin (MIC≥512μg/ml). Genes encoding aminoglycoside-modifying enzymes including ant(2″)-Ia, aac(6′)-Ib, aph(3′)-Ia, aac(3)-Iaand aph(3′)-VI, and 16S ribosomal RNA (rRNA) methylase armA, rmtA, rmtB, rmtC, rmtD,rmtE and npmA were detected by polymerase chain reaction (PCR), armA gene waspresent in 50% (52/104) of A. baumannii isolates with high-level resistance to aminoglycosides (MICs≥512 μg/ml). No rmtA, rmtB, rmtC, rmtD, rmtE or npmA genes were found. The rates of ant(2″)-Ia, aac(6′)-Ib, aph(3′)-Ia, aac(3)-Ia and aph(3′)-VI were 68.25%,20%,70%,47.5% and 1.25%, respectively. armA, ant(2″)-Ia and aph(3')-Ia genes coexisted in 62.5%(50/80) of aminoglycoside-resistant isolates, armA, ant(2″)-Ia and aac(6′)-Ib were commonly positive in same isolates. The presence of aminoglycoside-modifying enzymes was responsible for the moderate level resistance to aminoglycosides in A. baumannii, whereas armA was responsible for the high-level resistance to aminoglycosides. Aminoglycoside-resistant A. baumannii isolates were classified into genotypes by Random Amplified Polymorphic DNA PCR (RAPD-PCR), pattern A was almost throughout wards of the hospital. In summary, most A. baumannii is resistant to aminoglycosides, in the hospital coexistence of armA and genes encoding aminoglycoside-modifying enzymes are the main reasons. Key words: Acinetobacter baumannii, aminoglycoside-resistant, 16S rRNA methylase, aminoglycoside-modifying enzymes, RAPD-PCR

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